Abstract
Recent evidence suggests that blockade of normal excitation in the immature nervous system may have profound effects on neuronal survival during the period of natural cell death. Cell loss following depression of electrical activity in the central nervous system (CNS) may explain the neuropsychiatric deficits in humans exposed to alcohol or other CNS depressants during development. Thus, understanding the role of electrical activity in the survival of young neurons is an important goal of modern basic and clinical neuroscience. Here we review the evidence from in vivo and in vitro model systems that electrical activity participates in promoting neuronal survival. We discuss the potential role of moderate elevations of intracellular calcium in promoting survival, and we address the possible ways in which activity and conventional trophic factors may interact.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Action Potentials
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Afferent Pathways / physiology
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Animals
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Apoptosis
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Calcium Channels / metabolism
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Calcium Signaling
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Cell Survival
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Cells, Cultured
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Central Nervous System / drug effects
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Central Nervous System / embryology*
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Central Nervous System / physiology
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Chick Embryo
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Cyclic AMP / physiology
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Ethanol / pharmacology
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Ethanol / toxicity
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Excitatory Amino Acid Antagonists / pharmacology
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Female
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Fetal Alcohol Spectrum Disorders / etiology
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Fetal Alcohol Spectrum Disorders / pathology
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Fetal Alcohol Spectrum Disorders / physiopathology
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GABA-A Receptor Agonists
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Homeostasis
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Humans
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Ion Transport
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Mice
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Mice, Transgenic
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Models, Neurological
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Nerve Growth Factors / physiology
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Nerve Tissue Proteins / deficiency
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / physiology
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Neurons / cytology
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Neurons / physiology*
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Pregnancy
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Prenatal Exposure Delayed Effects
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Signal Transduction / drug effects
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Synaptic Transmission*
Substances
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Calcium Channels
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Excitatory Amino Acid Antagonists
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GABA-A Receptor Agonists
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Nerve Growth Factors
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Nerve Tissue Proteins
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Ethanol
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Cyclic AMP